In patients with moderate asthma whose symptoms are well-controlled by using an inhaled B-agonist on an "as needed" basis and an inhaled corticosteroid on a scheduled basis, continued treatment with the inhaled corticosteroid does not differ in efficacy from a change to therapy with a long-acting B-agonist. This null hypothesis was proposed to examine the importance of anti-inflammatory therapy in altering symptoms, airway function, and bronchial reactivity in patients with moderate asthma. This protocol is the third from the NIH funded Asthma Clinical Research Network, a multi-center network formed in 1993 to evaluate pathogenesis and treatment of asthma. This will be a 28-week, randomized, double-blind, prospective multi-center trial comparing in subjects with moderate asthma the efficacy of an inhaled corticosteroid (triamcinolone acetonide) with that of an inhaled long-acting B-adrenergic agonist (salmeterol xinafoate) and with placebo, during 16 weeks of therapy, and for 6 weeks following cessation of therapy. After a 6 week run-in period, during which they receive inhaled corticosteroid (triamcinolone, 4 puffs BID) and as needed rescue albuterol, subjects will be randomized to receive either the inhaled corticosteroid (triamcinolone, 4 puffs BID) or salmeterol (2 puffs BID) or placebo (2 puffs BID) for the next 16 weeks. All subjects will be provided with albuterol inhalers to use as rescue medication throughout the study. Subjects will take the study medication for 16 weeks, then stop medication for an additional 6 week single-blind study period to examine the "off effect" of the medications. Bronchoscopy with bronchoalveolar lavage and endobronchial biopsy will be performed prior to randomization and at the end of treatment. Induced sputum will be performed at four points during the study: baseline, prior to randomization, after treatment, and end of run-out. Physiologic outcome variables include forced expiratory volume in one second (FEV1) measured in the laboratory, peak expiratory flow rate measured at home and the provocative concentration of methacholine required to produce a 20% fall in lung function (PC20). Variables reflective of airway inflammation include the absolute and percentages of macrophages, neutrophils, lymphocytes and eosinophile in sputum, bronchoalveolar lavage and endobronchial biopsy.